Brain aging, Alzheimer's disease, and mitochondria

被引：245
作者：
Swerdlow, Russell H. [1 ,2 ,3 ]
机构：
[1] Univ Kansas, Sch Med, Dept Neurol, Kansas City, KS USA
[2] Univ Kansas, Sch Med, Dept Biochem & Mol Biol, Kansas City, KS USA
[3] Univ Kansas, Sch Med, Dept Mol & Integrat Physiol, Kansas City, KS USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2011年 / 1812卷 / 12期
关键词：
Aging; Amyloid; Brain; Dementia; Alzheimer's disease; Mitochondria; MILD COGNITIVE IMPAIRMENT; AMYLOID PRECURSOR PROTEIN; WHITE-MATTER LESIONS; OLDEST-OLD; AEROBIC GLYCOLYSIS; ASSOCIATION WORKGROUPS; DIAGNOSTIC GUIDELINES; NATIONAL INSTITUTE; CASCADE HYPOTHESIS; ENERGY-METABOLISM;
D O I：
10.1016/j.bbadis.2011.08.012
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The relationship between brain aging and Alzheimer's disease (AD) is contentious. One view holds AD results when brain aging surpasses a threshold. The other view postulates AD is not a consequence of brain aging. This review discusses this conundrum from the perspective of different investigative lines that have tried to address. it, as well as from the perspective of the mitochondrion, an organelle that appears to play a role in both AD and brain aging. Specific issues addressed include the question of whether AD and brain aging should be conceptually lumped or split, the extent to which AD and brain aging potentially share common molecular mechanisms, whether beta amyloid should be primarily considered a marker of AD or simply brain aging, and the definition of AD itself. (C) 2011 Elsevier B.V. All rights reserved.
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收藏
页码：1630 / 1639
页数：10
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